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Allergic skin diseases of the horse (Proceedings)
This is the most common allergic skin disease of the horse, caused by a hypersensitivity to the bites of common insects. There are a variety of common names for this condition including "sweet itch" and "summer eczema".
This is the most common allergic skin disease of the horse, caused by a hypersensitivity to the bites of common insects. There are a variety of common names for this condition including "sweet itch" and "summer eczema". This is thought to be a type 1 hypersensitivity reaction involving allergen specific IgE, but a delayed type hypersensitivity reaction may also be involved. Familial involvement can often be documented.
A. Etiology: Culicoides sp. (no-see-ums, midges), black flies, horse flies, horn flies, deer flies, mosquitoes, and stable flies. Culicoides sp. are the most common insects involved. There are as many as 1000 different species of Culicoides worldwide. The different species have different feeding preferences. Culicoides feed most at dusk and dawn and prefer environments with much standing water, decaying vegetation, and manure. They are poor fliers, and have a limited flight range (1-2 km).
B. Clinical Signs: whether due to Culicoides or other insects, this is characterized by a seasonal pruritus. Distribution of lesions may differ depending on the species of insect involved. Different species of Culicoides gnats prefer different areas of the body. The most common being the topline (mane, tail, ears, back) and ventrum. Horn flies tend to feed on the ventral abdomen, mosquitoes on the lateral aspects of the body, black flies on the head, ears, and ventrum, and stable flies on the lower limbs, ventrum, chest, and back. The dermatitis is characterized initially by crusted papules or wheals followed by by excoriation, scaling, and self trauma; the mane and tail may become broken and matted from self trauma. Secondary infections are common.
1. History of seasonal occurrence
2. Clinical signs
3. Response to insect control
4. Biopsy: Nondiagnostic . . . typical allergic response
5. Intradermal allergy testing for each individual species of insect.
D. Differential Diagnoses:
1. Atopic dermatitis
5. Ectoparasites (mange, chiggers, etc)
E. Treatment: Culicoides Avoidance Measures "Separate the bug from the horse"
1. Insect control: For Culicoides - Stable during dawn and dusk with very fine meshed netting ( smaller than mosquito netting).
2. Decrease standing water or move horse further than 2 km from standing water
3. Frequent spraying of horse with insect repellants (pyrethroids, Avon skin so soft) or timer operated spray misters in the stalls.
4. Box fans in the stalls – Culicoides gnats are poor fliers.
5. Co2 producing insect traps (Mosquito magnet)
6. Full body suits
7. Cattle tags with fenvalerate or pyrethrins (extralabel)
F. Treatment: Symptomatic
1. Corticosteroids: Prednisone 1 mg/kg PO SID x 1-2 weeks then taper off.
2. Antihistamines and fatty acids may be of benefit (see atopic dermatitis section)
3. Immunotherapy – very successful in one study, not effective in another.
A hypersensitivity disorder in which the horse becomes sensitized to inhaled or percutaneously absorbed allergens such as pollens, molds, and dust.
A. Pathogenesis:Atopy is classified as a type 1 hypersensitivity reaction. Allergens enter the body from inhalation or percutaneous absorption and bind to allergen-specific IgE antibodies on the surface of mast cells in the skin. This results in mast cell degranulation and release of a wide variety of inflammatory mediators (e.g. histamine, heparin). It is known in humans, dogs, and rodents that atopic individuals tend to produce a T helper 2 (TH2) lymphocyte response to allergens. TH2 cells produce cytokines such as IL4, Il5, IL6, IL10, and IL13 which help to promote antibody production of B lymphocytes. IL4 and IL13 are essential for the B cell immunoglobulin class switch to IgE. In nonatopic animals, a TH1 response to environmental allergens is produced. Cytokines from TH1 cells can suppress the proliferation of TH2 cells and inhibit IgE production.
Studies have shown that horses affected with COPD have significantly higher levels of allergen-specific IgE in their bronchoalveolar lavage fluid than normal horses.
B. History/Clinical signs: Seasonal or nonseasonal pruritus of the face, ears, ventrum, and legs. Recurrent, pruritic or non-pruritic urticaria. .Respiratory disease (e.g. COPD) and head shaking (rarely) may also be manifestations of atopy. Onset of clinical signs is most commonly seen at 1.5 to 4 years of age. Familial predisposition. Thoroughbreds and Arabians are predisposed. Secondary lesions may include excoriations, lichenification, hyperpigmentation, and alopecia. Secondary bacterial infections are common.
C. Differential Diagnoses
1. Insect hypersensitivity
3. Allergic/irritant contact dermatitis
4. Food allergy
5. Cutaneous drug eruption
a. History and clinical signs
b. Intradermal allergy testing (IDAT)
c. There is no single test that can definitively diagnose atopy. It is important to rule out other possible causes of the clinical signs,and gather information through the history, physical examination, response to various medications (e.g. steroids, antihistamines), and results of intradermal allergy testing. Histopathology may be supportive.
Serological allergy tests are commercially available. There are currently no published validation results for the commercially available ELISA tests for equine allergies, and there are enormous problems with accuracy and repeatability. They are far less reliable than the similar canine assays, and are much more expensive. Response to immunotherapy based on serological test is poor.
Intradermal allergy testing is the test of choice to aid in the diagnosis and treatment (via immunotherapy) in the allergic horse. This should be performed by a veterinary dermatologist or other veterinarian with experience in performing and interpreting skin tests. Appropriate drug withdrawals are needed prior to IDAT: Oral steroids – 3 weeks. Long acting injectable steroids – 6 weeks. Antihistamines – 10 days. Acepromazine – 2-3 days. These withdrawal times are not "set in stone" and I find that some horses can be tested with much shorter withdrawal times.
a. Prednisone/prednisolone 1-2 mg/kg q 24 hrs for 3-7 days then on alternate days. The dose should then be tapered to the lowest possible alternate day dose that controls the clinical signs.
b. Dexamethasone 0.05 -0.2 mg/kg for 3-7 days, then on alternate days. The dose should then be tapered to the lowest possible q 72 hr dose that controls the clinical signs.
Hydroxizine HCL or pamoate: 400-600 mg/horse 2-3 times per day – $$, Hydroxizine pamoate is less expensive and likely as effective.
Chlorpheniramine 200 mg/horse BID
Diphenhydramine 300-400 mg/horse BID
Doxepin 300-400 mg/horse BID
Must withdraw prior to most shows or competitions
4. Fatty acids
a. Derm caps 100s 3-5 caps BID
5. Topical antipruritics (oatmeal or pramoxine shampoos, corticosteroids)
6.Immunotherapy (based on IDAT) – THE ONLY SPECIFIC TREATMENT
Underutilized therapy in equine medicine
Injections given every 2-3 weeks.
Dose is the same as for a dog – very cost effective
No drug residues for competitive/show horses
Success rates (good to excellent response)
Atopic/pruritic horses = 75%
Chronic atopic urticaria = 80-90%, recent studies - (13/14, 92%) and (6/6, 100%)
COPD horses = 67 – 86% in two studies
Head shaking = ~50%
7.Control secondary infections
8. Adequate insect control if concurrent insect hypersensitivity
This is a manageable, not curable disease.
Edematous skin disorders leading to papules or nodules which may or may not be pruritic. May be immunologic or nonimmunologic in nature. Urticaria is more common in the horse than any other domestic species.
A. Pathogenesis: Degranulating mast cells and basophils release inflammatory mediators resulting in dermal edema. Immunologic causes usually involve a type I hypersensitivity. Non immunologic causes usually involve a physical trigger or stressor.
1. Allergies – insects, atopy, foods, contact.
2. Drugs, vaccines
3. Physical factors – cold, heat, pressure (dermatographism), exercise
5. Idiopathic – A definitive diagnosis is found in only 25% of human cases of chronic urticaria.
1. Urticarial lesions can occur anywhere on the body, esp. the trunk, and neck.
2. Papules, nodules or plaques in a variety of patterns.
3. Pit on digital pressure.
4. Are transient, last <than 24-48 hours.
5. Considered chronic if lasts longer than 8 weeks.
6. Angioedema – very large edematous swellings most commonly on the muzzle and eyelids. May be on the neck, ventrum and distal extremities. May leak serum or blood.
7. Angioedema is often secondary to drug reaction (esp. Procaine penicillin G), other causes include snake bites, and ingested plant proteins.
1. Detailed history
2. Physical exam
3. If persist in one spot longer than 48 hrs, probably not hives. Ddx: erythema multiforme, neoplasia (lymphoma), amyloidosis, dermatophytosis, folliculitis, eosinophilic granulomas.
4. Biopsy – may rule out other causes, but generally unrewarding.
5. Rule out the known causes of urticaria through process of elimination based on history and exam. Refer for intradermal allergy testing (IDAT) if atopy and/or insect hypersensitivity is suspected.
E. Treatment: (Dependent on underlying cause. See atopy section)
1. Avoidance of offending substance
2. Antihistamines (Hydroxizine most effective)
4. Immunotherapy if indicated based on Intradermal allergy testing ( highly effective).
An allergic or idiosyncratic reaction to grains, grasses, supplements or food additives. Usually nonseasonal, but can be seasonal if pasture plants are the cause. No age predilection. Rare. May be caused by Type I, Type III, and Type IV hypersensitivity reactions.
A. Offending substances: oats, wheat, barley, bran, alfalfa, feed additives
B. Clinical Signs: Pruritus of the face, neck, trunk, and tail area. Some horses are only "tail rubbers". Pruritic or nonpruritic urticaria.
1. Elimination diet for 4 weeks. (e.g. all grass hay – timothy). If improvement is seen, the horse should then be re-challenged with the suspected foodstuff and watch for an increase in pruritus.
2. Serological tests (RAST, ELISA) are available and have zero value. These are not recommended.
3. IDAT is also not known to be accurate.
D. Treatment: Avoidance of the offending substance.
Lorch, G., Hillier, A. et. al. Results of intradermal tests in horses without atopy and horses with atopic dermatitis or recurrent urticaria. Am J Vet Res 62, 1051-1059.
Lorch, g. Hillier, A. et. al. Comparison of immediate intradermal test reactivity with serum IgE quantitation by the use of a radioallergosorbent test and two ELISA in horses with and without atopy. J Am Vet Med Assoc 219, 1314-1322.
Tallarico, N.J., Tallarico, C.M. (1998) Results of intradermal allergy testing and treatment hyposensitization of 64 horses with chronic obstructive pulmonary disease, urticaria, head shaking, and/or reactive airway disease. Veterinary Allergy and Clinical Immunology.
Jose-Cunilleras, E., Kohn, C.W., et al. (2001) Intradermal testing in healthy horses with chronic obstructive pulmonary disease, recurrent urticaria, or allergic dermatitis. J Am Vet Med Assoc 219, 1115-1121.
Scott, D.W., Miller, W.H. (2003) Skin Immune System and Allergic Diseases. In: Equine Dermatology, Saunders, St. Louis. pp 395-474.
Morris, D.O, Lindborg, S. (2003) Determination of 'irritant' threshold concentrations for intradermal testing with allergenic insect extracts in normal horses. Vet Dermatol